arXiv subjects

Lior Atia

Publications and source records attributed to Lior Atia.

4 recordsLinked to original sources

arXiv2025

Local shear induces long-range suppression of cellular motion in stiff epithelial monolayers

As small particles skim our airways during breathing, or our intestines during digestion, the surface epithelium is subjected to local exogenous shear that deforms hundreds to thousands of tightly interacting cells. Unlike shear deformations applied at the macro-tissue scale or the micro-cell scale, the effects of such perturbations at the meso-scale remain largely unexplored. To address this, we developed a mesoscopic probe that adheres to the apical surface of an epithelial monolayer and applies magnetically driven local shear. We find that localized shear suppressed cellular migratory dynamics far beyond the immediate neighbors in stiffer layers, whereas in softer layers the same perturbation produced no detectable long-range change in dynamics. This mechano-transductive relationship is further supported by unconfined mature layers, in which increased stiffness was accompanied by restored shear responsiveness. Viewed at the level of collective dynamics, shear-induced migratory suppression in stiff layers was often accompanied by reduced MSD scaling exponents and changes in cell shape, but these responses were not fully captured by the epithelial jamming framework. Together, these observations provide a new perspective on how a local mechanical perturbation traverses the epithelial monolayer to influence both nearby and distant cellular environments.

physics.bio-ph↗

arXiv2025

Cell Shape Emerges from Motion

We perform cell segmentation on images from experimental studies of confluent, mobile cells in epithelial monolayers and show that these systems possess a broad, positively-skewed shape parameter distribution $P(\mathcal{A})$, where $\mathcal{A}=p^2/4\pi a$, $p$ is the perimeter, and $a$ is area of each cell. $P(\mathcal{A})$ is peaked at a value higher than the typical shape parameter $\mathcal{A}^* \sim 1.15$ that occurs for randomly packed, static confluent cell monolayers. The distribution does not arise from a heterogeneous population of cells with different fixed $\mathcal{A}$, nor can it arise from cell shape fluctuations from strains below the elastic limit. Instead, we find that all cells in each monolayer sample $\mathcal{A}$ values that span the full shape parameter distribution. We develop a deformable particle model that allows cell perimeter to adapt to local forces during cell motion, and this model recovers $P(\mathcal{A})$ to within $5\%$ for both MDCK and HaCaT epithelial cell monolayers. These results emphasize that confluent epithelial monolayers of mobile cells generate a well-defined broad shape parameter distribution that is independent of the initial cell shapes.

cond-mat.soft↗

arXiv2025

A self-organized compression network arrests epithelial proliferation

As epithelial development or wound closure approaches completion, cell proliferation progressively slows via contact inhibition of proliferation (CIP) - a mechanism understood as being strictly local. Here we report the discovery of inhibition of proliferation through an unanticipated mechanism that is non-local. As a confluent epithelial layer becomes progressively more jammed, two interpenetrating networks emerge: islands of mechanically compressed non-cycling cells percolating within an ocean of mechanically tensed cycling cells. The evolution of the compression network was found to be susceptible to both specific molecular stimulus and to injury-induced unjamming. Yet, in all circumstances, the size of compressed islands followed a power-law distribution that was well-captured by preferential network theory. Together, these findings demonstrate the existence of a network-based inhibition of proliferation (NIP) that is self-organizing and poised in proximity to criticality.

q-bio.CB↗

arXiv2017

Universal geometric constraints during epithelial jamming

As an injury heals, an embryo develops, or a carcinoma spreads, epithelial cells systematically change their shape. In each of these processes cell shape is studied extensively, whereas variation of shape from cell-to-cell is dismissed most often as biological noise. But where do cell shape and variation of cell shape come from? Here we report that cell shape and shape variation are mutually constrained through a relationship that is purely geometrical. That relationship is shown to govern maturation of the pseudostratified bronchial epithelial layer cultured from both non-asthmatic and asthmatic donors as well as formation of the ventral furrow in the epithelial monolayer of the Drosophila embryo in vivo. Across these and other vastly different epithelial systems, cell shape variation collapses to a family of distributions that is common to all and potentially universal. That distribution, in turn, is accounted for quantitatively by a mechanistic theory of cell-cell interaction showing that cell shape becomes progressively less elongated and less variable as the layer becomes progressively more jammed. These findings thus uncover a connection between jamming and geometry that is generic -spanning jammed living and inert systems alike- and demonstrate that proximity of the cell layer to the jammed state is the principal determinant of the most primitive features of epithelial cell shape and shape variation.

physics.bio-ph↗